Biology and management of freesia flower specking caused by Botrytis cinerea

There is no published research regarding postharvest infection of freesia flowers by Botrytis cinerea. Although, infection problems have concerned freesia growers and wholesalers in recent years. The overall objectives of this study were firstly to evaluate the factors affecting B. cinerea postharvest disease establishment and secondly to evaluate a range of novel potential treatments to reduce postharvest freesia infection. These treatment options include plant activators such as acibenzolar-S-methyl and methyl jasmonate and biotic (Aureobasidium pullulans) and abiotic (UV-C irradiation) biological/elicitors agents. Research was undertaken in an attempt to explain the variation in B. cinerea incidence on cut freesia flowers as noted by the UK importer Zwetsloots & Sons Ltd. in 2000. Higher monthly rejections of freesia flower stems throughout 2000 due to B. cinerea infection were recorded during spring (April-May), early summer (June) and autumn (October). Comparatively higher proportions of rejected freesia stems were associated with glasshouse temperatures ranging from 13-17°C. In the presence of B. cinerea inoculum on freesia petal surface, temperature was not a limiting factor for disease establishment. Incubation of artificially inoculated freesia flowers at 12°C resulted in overall higher disease severity and lesion numbers compared to flowers incubated at 5 or 20°C. In contrast, relative humidity was the most important factor for postharvest infection by B. cinerea. Elicitor based strategies for IPM using the potent activator acibenzolar provided limited protection of freesia flowers against B. cinerea when applied postharvest. Acibenzolar significantly reduced disease severity, lesion numbers and lesion diameters compared to the untreated control when applied at 0.15 g A. 1. U1. Methyl jasmonate (MeJA) applied as gas, pulse and spray generally suppressed B. cinerea disease on cut freesia flowers. Disease severity, lesion numbers and lesion diameters of flowers gassed with 0.1 μL MeJA L"' were reduced by 56,43 and 37%, respectively compared to untreated control flowers. Gaseous MeJA treated freesia flowers at 0.1 μL L"1 increased PPO activity by 57% compared to untreated controls 24h after MeJA treatment. After 36h of incubation at 20°C, disease severity, lesion numbers and lesion diameters of gaseous MeJA treated flowers were reduced by 68,56 and 50%, respectively, compared to the untreated controls. However, PAL activity in MeJA treated freesia flowers did not decrease significantly over time compared to untreated control 12h post-inoculation and thereafter. These findings suggest that MeJA treatment might suppress the action of PAL in the phenylpropanoid pathway and consequently block SA production. UV-C irradiation might be used in an integrated postharvest disease management program for freesia flowers. UV-C irradiation after artificial inoculation resulted in markedly reduced B. cinerea disease severity scores and lesion numbers. In detail, UV-C irradiation of cut freesia flowers with 0.5,1,2.5 and 5 kJ m''reduced disease severity by up to 44,70,74 and 59% and lesion numbers by up to 37,62,68 and 60%, respectively. UV-C irradiation at 1 kJ M-2 before artificial inoculation slightly reduced disease severity and lesion numbers possibly by inducing defence responses. However, the limited disease suppression suggested that apparently B. cinerea could overcome the UV-C induced effect. The effect of preharvest treatments on freesia crops with acibenzolar was investigated in glasshouse trials in view to suppress postharvest B. cinerea infection via SAR induction. Acibenzolar was effective in selected treatments and conditions. Disease pressure varied over the 3 years and over varieties tested. However, it was unclear whether acibenzolar induced systemic and/or local defence responses. The latter was supported by biochemical investigations in 2001 which suggested that acibenzolar did not induce PAL activity. In contrast, preharvest MeJA treatment resulted in markedly systemic protection of treated flowers compared to untreated ones. MeJA efficacy was dependent on variety and on postharvest incubation temperatures. Disease severity, lesion numbers and lesion diameters on MeJA treated freesia var.Dukaat' flowers incubated at 20°C were reduced by 56,61, and 49% compared to controls, respectively. Also, disease severity, lesion numbers and lesion diameters on MeJA treated `Cote d'Azur' flowers incubated at 20°C were reduced by 36,26, and 49% compared to controls, respectively.